Spath S Becher B 2013 The search for the encephalitogenic factor driving pathogenic T cells in autoimmune diseases such as rheumatoid arthritis, multiple sclerosis (MS), and psoriasis has proven to be a long and difficult mission, which is not yet completed. In this issue of the European Journal of Immunology, the importance of the transcription factor T-bet, previously shown to be essential for the induction of autoimmune disease in mice, is challenged. Two independent groups, O'Connor et al. [Eur. J. Immunol. 2013. 43:2818-2823] report] and Grifka-Walk et al. [Eur. J. Immunol. 2013. 43:2824-2831], report that T-bet is not mandatory for T cells to cause experimental autoimmune encephalomyelitis (EAE), which serves as a paradigmatic T-cell-mediated autoimmune disease. Both groups found that T-bet KO mice were fully susceptible to develop EAE, both after immunization with self-antigen and after adoptive transfer of IL-23-polarized autoaggressive T cells. T-bet deficiency mediated the loss of IFN-γ expression but retained or even enhanced GM-CSF and IL-17 production by central nervous system (CNS)-infiltrating T cells. These findings indicate that we have lost the last transcriptional regulator previously held to be required for the generation of autoimmune pathogenic T cells. application/pdf https://sonar.ch/global/documents/209305 eng info:eu-repo/semantics/altIdentifier/doi/10.1002/eji.201344109 info:eu-repo/semantics/altIdentifier/pmid/24142468 info:eu-repo/semantics/openAccess European journal of immunology. - 2013 Autoimmunity EAE GM-CSF IL-17 IL-23 T-bet Transcription factors Animals Encephalomyelitis, Autoimmune, Experimental T-Box Domain Proteins Th1 Cells Th17 Cells T-bet or not T-bet: taking the last bow on the autoimmunity stage. http://purl.org/coar/resource_type/c_6501